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Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
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Recent advances in autoimmune encephalitis.

João Henrique Fregadolli Ferreira1, Caio César Diniz Disserol1,2,3, Bruna de Freitas Dias1

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Summary

Autoimmune encephalitis (AE) research has expanded beyond N-methyl-D-aspartate receptor antibodies (anti-NMDARE) to include over 12 new syndromes. This review covers advances in AE pathophysiology, genetics, diagnosis, and clinical features, offering updated diagnostic criteria and assessment tools.

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Area of Science:

  • Neurology
  • Immunology
  • Genetics

Background:

  • Autoimmune encephalitis (AE) encompasses syndromes targeting cell surface antibodies and anti-GAD.
  • Since 2007, over 12 new AE-associated antibodies and clinical syndromes have been identified.
  • Research has advanced understanding of pathophysiology, genetics, diagnosis, and clinical phenotypes.

Purpose of the Study:

  • To review recent advances in AE pathophysiology, genetics, diagnosis, and clinical phenotypes.
  • To highlight genetic associations (HLA) for specific antibodies.
  • To update diagnostic criteria and propose an algorithm for AE, especially in pediatric populations.

Main Methods:

  • Literature review of recent advances in autoimmune encephalitis.
  • Analysis of genetic studies reporting HLA associations.
  • Characterization of cognitive, psychiatric, and sleep disorders in AE patients.
  • Review of diagnostic criteria, algorithms, and assessment scales.

Main Results:

  • Human leukocyte antigen (HLA) associations identified for anti-LGI1, anti-Caspr2, anti-IgLON5, and anti-GAD antibodies.
  • Expanded clinical spectrum for anti-LGI1, anti-AMPAR, anti-CASPR2, and anti-IgLON5.
  • Late-onset anti-NMDARE and anti-GABA-BR encephalitis show worse prognoses and distinct tumor associations.
  • Updated diagnostic criteria and algorithms proposed, addressing pediatric AE and potential mimics.

Conclusions:

  • AE research has significantly expanded beyond anti-NMDARE, revealing diverse clinical presentations and genetic links.
  • Revised diagnostic approaches and assessment tools are crucial for accurate AE management.
  • Further research is needed to address limitations in commercial assays and refine treatment strategies.